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PubMed1988

Role of the coagulation system in tumor-cell-induced platelet aggregation and metastasis.

The ability of tumor cells to initiate coagulation and subsequent platelet aggregation is believed to facilitate the metastatic process. The mechanism by which tumor cells initiate thrombotic alterations is unclear. We have purified a plasma membrane protein platelet aggregating activity/procoagulant activity (PAA/PCA) from several rodent tumors which initiates the coagulation of homologous plasma and aggregation of homologous platelets by a mechanism independent of factor VII. This protein does not possess any proteinase activity; however, its activity is dependent upon the presence of factor X. In addition, PAA/PCA requires reconstitution with phospholipid for expression of activity. These results suggest that tumor cells express a unique protein which possesses procoagulant activity resulting in thrombin generation. Thrombin is responsible for subsequent tumor-cell-induced platelet aggregation.

Amino Acids↗
PubMed2001

Regulation of platelet aggregation in vitro by plasma adenosine in preeclampsia.

The aim of this study was to evaluate the possible role of plasma adenosine in platelet aggregation in preeclampsia. We measured the plasma adenosine concentration [ADO] and in vitro platelet aggregation in the third trimester of normal pregnant (n = 15) and preeclamptic women (n = 15). The mean plasma [ADO] in preeclampsia was 0.68 +/- 0.08 microM (means +/- SEM), significantly higher than in normal pregnancy (0.42 +/- 0.09 microM) (p < 0.05). In preeclampsia, platelet aggregation in response to collagen was approximately 40% lower than that in normal pregnancy (p < 0.05). There was an inverse correlation between the plasma [ADO] and platelet aggregation in vitro (r = -0.27, p < 0.05). These results suggest reduced platelet aggregation in preeclampsia may be at least in part attributed to an elevation of the the plasma [ADO].

Adenosine↗
PubMedDate not supplied

[Effect of ultrafiltrates in plasma from patients with chronic uremia on platelet aggregation].

An effect of 20 ultrafiltrates from patients with chronic renal failure on ADP-, epinephrine-, and arachidonic acid-induced platelet aggregation. Ultrafiltrates were collected at the beginning and the end of dialysis. It was found that ultrafiltrates collected at the beginning of dialysis decrease ADP-induced platelet aggregation whereas ultrafiltrates collected at the and of dialysis exert reverse effect. No effect on epinephrine- and arachidonic acid-induced platelet aggregation was seen. Removal of substances inhibiting platelet aggregation produced by ADP hemodialysis may reveal increased platelet aggregation in patients with uremia.

Adolescent↗
PubMed1980

Platelet aggregation related to age in diabetes mellitus.

Platelet aggregation induced by ADP and collagen was studied in 174 diabetic patients before entering a controlled clinical trial. The clinical characteristics have been precisely defined. The degree of retinal abnormality was assessed by fundus angiofluorography in every patient. Most patients had background retinopathy; the remainder were normal. All results were computer analysed. The only significant relationship observed was between platelet sensitivity to ADP which increases regularly in relation to age in both insulin- and non-insulin-treated diabetic patients with or without background retinopathy. Spontaneous platelet aggregation was observed in 13 subjects and was not correlated to the existence of a neuropathy or any other clinical characteristics.

Adenosine Diphosphate↗
PubMed1980

Platelet-membrane fatty acids, platelet aggregation, and thromboxane formation during a mackerel diet.

Eicosapentaenoic acid (C20:5 omega 3), which is present in high concentration in certain salt-water fish, may reduce the incidence of cardiovascular disease in Greenland Eskimos by reducing platelet aggregation and adhesion. Changes in platelet and plasma fatty acids, platelet aggregation, and thromboxane (TX) formation were studied in 7 healthy White men who had been on a mackerel diet for 1 week. Platelet aggregation had TX synthesis after low-dose collagen stimulation in platelet-rich plasma were reduced. This could be due to the marked change of the ratio of C20:5 to arachidonic acid (C20:4 omega 6) in platelet membranes. When the men were on the mackerel diet, their C20:5 level in platelet membranes and in plasma increased and that of C20:4 dropped. Both fatty acids were released during platelet aggregation. The reduction in the amount of C20:4 liberated and/or a diminished conversion of C20:4 to TXA2 by competitive inhibition of the platelet cyclo-oxygenase by the released C20:5 could be responsible for the decreased platelet aggregation.

Animals↗
PubMed1995

Conditions that lithium inhibits or potentiates vasopressin V1-receptor-mediated platelet aggregation and [Ca++]i mobilization.

1. Besides clinical use, there are many explanations for the mechanism of action of lithium. Although it is shown that lithium may reduce the supply of inositol that is required to sustain phosphoinositide synthesis, evidence exists concerning the potentiating effect of lithium on this pathway. We therefore decided to evaluate conditions in which lithium inhibits or potentiates platelet aggregation and calcium response induced by vasopressin. 2. Platelet aggregation was measured by the photometric method, and changes in intracellular free calcium were measured using fura-2/AM. 3. We show an inhibitory action of neomycin on vasopressin-induced platelet aggregation. Lithium, according to the preincubation time, could both potentiate or inhibit platelet aggregation and calcium responses induced by vasopressin. The inhibitory effect of lithium on platelet aggregation is dependent on concentrations of both lithium and vasopressin and also the presence of indomethacin, for example, in the absence of indomethacin there was no clear inhibitory action of lithium on vasopressin-induced platelet aggregation. 4. These results show the importance of arachidonate metabolites concerning lithium effects on platelet V1-receptor signaling. In conclusion, because the arachidonate metabolites are responsible for the release of other active substances from platelets' granules, the aggregatory responses in the absence of indomethacin may be amplified, and this subsequently may change the net inhibitory action of lithium.

Arachidonic Acid↗
PubMed2003

Integrin alphaIIbbeta3-specific synthetic human monoclonal antibodies and HCDR3 peptides that potently inhibit platelet aggregation.

The interaction of fibrinogen with integrin alphaIIbbeta3 (GPIIb/IIIa), in part mediated by an RGD tripeptide motif, is an essential step in platelet aggregation. Based on their inhibition of platelet aggregation, three integrin alphaIIbbeta3 inhibitors are clinically approved. The clinically most widely used integrin alphaIIbbeta3 inhibitor abciximab is a chimeric mouse/human antibody that induces thrombocytopenia, often severe, in 1-2% of patients due to a human anti-mouse antibody (HAMA) response. In addition, unlike other ligands mimicking small molecular drugs, abciximab cross-reacts with integrin alphavbeta3 and alphaMbeta2. Here we used phage display to select monoclonal antibodies specific to integrin alphaIIbbeta3 from a synthetic human antibody library based on the randomized HCDR3 sequence VGXXXRADXXXYAMDV. The selected antibodies revealed a strong consensus in HCDR3 (V(V/W)CRAD(K/R)RC) and high specificity toward integrin alphaIIbbeta3 but not to other RGD binding integrins such as alphavbeta3, alphavbeta5, and alpha5beta1. The selected antibodies as well as three synthetic peptides (VWCRADRRC, VWCRADKRC, and VVCRADRRC) whose sequences were derived from the HCDR3 sequences of the selected antibodies strongly inhibited the interaction between integrin alphaIIbbeta3 and fibrinogen and platelet aggregation ex vivo. To our knowledge, these are the first fully human monoclonal antibodies that are specific to integrin alphaIIbbeta3 and can potently inhibit platelet aggregation.

Amino Acid Motifs↗
PubMed2001

Influence of hypotensive and normotensive anesthesia on platelet aggregability and hemostatic markers in orthognathic surgery.

This prospective randomized study investigated the influence of normotensive and hypotensive general anesthesia on platelet aggregability, intraoperative blood loss and parameters of plasmatic coagulation during extensive orthognathic surgery. A total of 30 patients were randomly allocated for either normotensive anesthesia maintained by continuous infusion of propofol and remifentanil (NORMO, n=10) or hypotensive anesthesia, whereby hypotension was induced by increasing the infusion rate of remifentanil (HYPO-R, n=10) or by administration of nitroglycerin (HYPO-N, n=10). Whole blood platelet aggregability was significantly reduced during hypotension compared to normotensive anesthesia (P<.01, HYPO-N and HYPO-R vs. NORMO). Mean arterial blood pressure during hypotension correlated well with adenosinediphosphate- (R=.712, P<.001) and collagen-induced platelet aggregability (R=.685, P<.001). Within hypotensive study groups, postoperative fibrinogen levels were significantly different, whereas intraoperative platelet aggregability, postoperative platelet count, prothrombin time, activated partial thromboplastin time and antithrombin levels were not different. Normotensive anesthesia, however, caused significant decreases in platelet count (-29%), prothrombin time (-24%), fibrinogen (-41%) and antithrombin (-28%) and a significant prolongation in activated partial thromboplastin time (+21%) and thrombin time (+18%). There was a trend to reduced intraoperative blood loss in hypotensive study groups; however, differences were not significant. In conclusion, induced hypotension--independent of substances used for induction of hypotension--reduces intraoperative platelet aggregability, subsequently protecting the coagulation system against subclinical consumption coagulopathy. Induced hypotension-caused platelet dysfunction does not lead to an increased intraoperative blood loss, but quite on the contrary shows a trend to reduced intraoperative blood loss, possibly by preventing platelet-induced subclinical consumption coagulopathy.

Adult↗
PubMed1982

Platelet aggregation in focal cerebral ischemia -a clinical study.

In a consecutive series of 35 patients with transient ischemic attacks (TIAs) 26 patients (74%) had pathological platelet aggregation 4 weeks after the latest TIA. Pathological platelet aggregation was the most frequent factor leading to a prophylactic treatment of the TIAs. Among 12 patients with reversible ischemic neurological deficit (RIND) only one had pathological platelet aggregation, and among 54 patients with completed stroke 37% had pathological platelet aggregation 4 weeks after the cerebral infarction. It is possible by the antiaggregating agents acetylsalicylic acid and dipyridamole to normalize in vitro pathological platelet aggregation. The frequency of side effects was low. During this treatment further TIAs were stopped in 17/19 patients, and remission were seen in 14/14 stroke patients. Compared with the remissions during treatment with anticoagulants there was a tendency of more favourable outcome in the group of stroke patients when treated with antiaggregating agents.

Adult↗
PubMed1988

A novel property of an aqueous guaraná extract (Paullinia cupana): inhibition of platelet aggregation in vitro and in vivo.

Aqueous extracts of guaraná were studied in terms of effects on the aggregation of human and rabbit platelets. Guaraná extracts have anti-aggregatory and de-aggregatory actions on platelet aggregation induced by ADP or arachidonate but not by collagen. The active material was shown to be water soluble and heat resistant and appeared to be different from salicylates, nicotinic acid or known xanthines. Guaraná extracts inhibited platelet aggregation in rabbits following either intravenous or oral administration.

Adenosine Diphosphate↗
PubMed1975

Platelets fixed with paraformaldehyde: a new reagent for assay of von Willebrand factor and platelet aggregating factor.

Present methods for assay of platelet aggregating agents use freshly prepared platelets. Much time is spent in daily preparation of platelets and standardization presents problems. The preparation of fixed washed platelets (FWP) and their use in two bioassays are described in this report. Washed human platelets were fixed for 48 hours with 4 per cent paraformaldehyde, washed twice in phosphate buffer, pH 6.4, and stored at 4 degrees C. Aggregation of FWP was studied with a macroscopic test and a light absorbance measurement. FWP did not aggregate with adenosine diphosphate, collagen, adrenalin, and thrombin. FWP aggregated with bovine or porcine plasma, poly-L-lysine, and ristocetin with normal human plasma but not with von Willebrand's disease plasma. These observations confirm the direct aggregating effect of these agents. Macroscopic aggregation times were dependent on the amount of aggregating agent (bovine plasma, normal human plasma). A quantitative assay for bovine platelet aggregating factor (PAF) and von Willebrand factor (vWF) with FWP was developed. The ability of FWP to aggregate remained unchanged after 1 month of storage at 4 degrees C. Ristocetin alone caused a decrease in light transmission of FWP suspensions, depending upon the concentration of ristocetin, but did not cause aggregation. FWP constitute a stable reagent suitable for quantitative measurement of PAF and vWF.

Animals↗
PubMed1998

[Observation on platelet aggregative ability in patients with malignant tumors of head and neck by electron microscope].

OBJECTIVE: To investigate the relationship between the platelet aggregative ability and malignant tumors of head and neck. METHOD: Platelet aggregative ability was detected by electron microscopy (EM) in 37 patients with malignant tumors of head and neck(Group C), 10 patients with non-neoplastic diseases(Group A) and 10 patients with benign tumors of head and neck(Group B) as the control group, with the ratio of aggregative type platelets as the index. Twenty-five of 37 patients with malignant tumors except 8 cases of nasopharyngeal carcinoma were included in the follow-up study 4-6 months after operations. RESULTS: 1. The mean ratio of aggregative type platelets in patients from Group C was significantly higher that that of Group A or Group B patients (P < 0.05); 2. In Group C, the mean ratio of aggregative type platelets increased significantly with the development of clinical staging(P < 0.05); 3. In follow-up study, the mean ratio of aggregative type platelets of 17 patients without metastasis and recurrence was significantly lower than that before-operation, while the results of 8 patients with metastasis or recurrence was totally opposite. CONCLUSIONS: 1. The aggregative ability of platelets increased in patients with malignant tumors of head and neck; 2. The ratio of aggregative type platelets detected by EM has an important potential value in judging the development, therapeutic effects and prognosis of the malignant tumors of head and neck.

Adult↗
PubMed2004

Design, synthesis, and inhibition of platelet aggregation for some 1-o-chlorophenyl-1,2,3,4-tetrahydroisoquinoline derivatives.

Based on ticlopidine active as an ADP receptor antagonist for inhibiting platelet aggregation in clinical test, and upon finding (+/-)-1,2-substituted-7-sulfonylamide/amide-1,2,3,4-tetrahydroisoquinoline (11-31) inhibited of platelet aggregation, a series of (+/-)-1-o-chlorophenyl-2-substituted-tetrahydroisoquinoline derivatives was designed and synthesized. Four analogs proved to be potential antiplatelet aggregation agents, and compound 9 (TQP-3, applying for patent) which inhibits ADP-induced human platelet aggregation with IC50 values of approximately 0.206 nM was the most active. Compound 2 is more active than compound 1, which (Type I) is similar to ticlopidine. This is because there is a spacial hindrance in compound 1, and the o-chloro group of compound 2 may play the same a role as o-chloro group of ticlopidine. On the other hand, with the different substitutions at different positions on the 2-substituted phenylacyl group, their inhibition of platelet aggregation differs. These compounds with m-substituted group (5, 7, 9) showed a higher IC50 value for inhibiting ADP-induced human platelet aggregation than those with o-substituted group (4, 6) or p-substituted group (3, 8). It was observed that their inhibition is bromine-substituted derivative (9), chlorine-substituted derivative (7), and nitro-substituted derivative (5) in turn. Moreover, these compounds (Type II) may be more similar to clopidogrel than to ticlopidine due to the acyl group at 2 position of the nucleus playing a role as the ester group of clopidogrel. It was conjectured that these analogs function as a potential antiplatelet aggregation role by acting as ADP receptor antagonists.

Adenosine Diphosphate↗
PubMed1994

Platelet aggregation inhibition by mononuclear leukocytes.

In this study we have investigated the effect of human mononuclear leukocytes (ML) on platelet aggregation. The results obtained demonstrated that coincubation of platelets with nonstimulated ML decreased platelet aggregation induced by collagen or thrombin in a concentration-dependent manner. The inhibitory effect increased with the incubation period of the cells, reaching a plateau at 5 minutes. T and non-T enriched ML suspensions exerted an inhibitory effect similar to the total population of ML. Supernatants from ML or mixed cell suspensions also diminished platelet aggregation. 6-keto PGF1 alpha concentration in the supernatants was less than 10 pg/ml. Hemoglobin, L-arginine and cytochrome C did not modify the antiaggregating activity of ML, whereas superoxide dismutase potentiated the inhibition of aggregation mediated by ML. The inhibitory effect was not modified by monoclonal antibody (MoAb) against the lymphocyte function-associated antigen 1, alpha subunit (LFA-1 alpha) or by a MoAb directed against P-selectin. Our results demonstrated that ML inhibited platelet aggregation, at least partially, by the release of a soluble factor(s) distinct of prostacyclin or nitric oxide. Surface adhesion molecules seem also not to be involved.

6-Ketoprostaglandin F1 alpha↗
PubMed1979

Effects of carbenicillin and phosphomycin on ADP induced platelet aggregation.

The effects of carbenicillin and phosphomycin separately or simultaneously, on ADP induced platelet aggregation have been studied in vivo. Platelet aggregation, ADP induced, was inhibited by carbenicillin and phosphomycin. The inhibition was proportional to the concentration of antibiotic. A slight inhibition was observed when platelet rich plasma was incubated simultaneously with both antibiotics, but synergy on the ADP-induced platelet aggregation was absent.

Adenosine Diphosphate↗
PubMed1991

In vitro inhibition of platelet aggregation by the liver with UW solution as the preservation fluid.

The influence of UW preservation fluid in comparison with that of Euro-Collins and Bretschneider solutions on collagen, adenosine diphosphate and ristocetin-induced platelet aggregation was investigated in vitro using platelet-rich plasma of 4 healthy volunteers. The concentrations of the solutions tested were comparable to those that may be used in the transplant situation. 2UW solution inhibited ADP and collagen-induced platelet aggregation--an effect that could be attributed mainly to adenosine and secondarily to penicillin in UW solution--whereas ristocetin-induced aggregation was not affected. Euro-Collins and Bretschneider solutions did not alter platelet aggregation. The inhibition of platelet aggregation by UW may, on the one hand, contribute to bleeding complications after reperfusion and, on the other hand, be responsible for the observed lower incidence of hepatic artery thrombosis.

Adenosine↗
PubMed2006

Aqueous extracts of Ocimum basilicum L. (sweet basil) decrease platelet aggregation induced by ADP and thrombin in vitro and rats arterio--venous shunt thrombosis in vivo.

OBJECTIVE: To study the effects of aqueous extract of Ocimum basilicum L (OBL) on platelet aggregation and experimental thrombus. METHODS: Platelet aggregation induced by ADP (5 muM) and thrombin (4 UI), and thrombus weight in an arteriovenous thrombosis (AVT) model were tested after 2 weeks treatment with 15, 75 and 375 mg/kg OBL orally in rats, compared to 8.8 mg/kg/day aspirin. AVT was also tested 2 h after 75 mg/kg OBL orally, after 3 and 7 days treatment, and one, three and seven days after the end of a two-week treatment. Analysis was done by ANOVA followed by protected t-tests (Tukey). RESULTS: OBL (15, 75, 375 mg/Kg) dose-dependently inhibits platelet aggregation by ADP and thrombin, with 75 mg/kg/day having approximately the same effect as 8.8 mg/kg/day aspirin. ADP induced aggregation reached 45%, 28% and 18% for OBL, respectively, 15, 75, 375 mg/kg compared to 71% for control and 27% for aspirin (all p<0.01 except aspirin vs. OBL 75 mg/kg/day p=0.7). Thrombin-induced aggregation reached 33%, 22%, 21% for OBL, respectively, 15, 75, 375 mg/kg compared to 67% for control and 48% for aspirin (all p<0.01 except OBL 75 vs. OBL 375 mg/kg/day, p=1.0). Compared to a control thrombus weight of 48.1 mg (SD 4.9), thrombus weight was 29.4 (3.3), 19.0 (1.9) and 12.3 (1.7) after treatment for 2 weeks with 15, 75 and 375 mg/kg OBL, respectively, and 27.4 (5.3) after 8.8 mg/kg aspirin (all p<0.001 except aspirin vs. OBL 75 mg/kg/day p=1.0). Maximum effect of OBL was reached after one week's treatment. The effect subsided between 3 and 7 days. CONCLUSION: OBL possesses an inhibitory effect on platelet aggregation induced by ADP and thrombin, that is dose-dependent and results in an anti-thrombotic effect in vivo which develops progressively over 7 days and disappears over 3-7 days. The active ingredient now needs to be characterized.

Adenosine Diphosphate↗
PubMed2000

Effects of MN-9202 on platelet aggregation, 5-HT release, TXB2 synthesis, and calcium mobilization in rabbit platelets in vitro.

AIM: To study the effects of MN-9202, a new effective Ca2+ channel blocker, on platelet aggregation, 5-HT and TXB2 release, and calcium transport induced by platelet activators. METHODS: The mobilization of cytosolic-free calcium induced by thrombin in washed platelets was observed by Ca(2+)-sensitive fluorescent indicator, Fura-2 AM and time scan measurement. Aggregation induced by ADP and thrombin in rabbits citrate platelet-rich plasma (PRP) was measured by aggregometer. 5-HT and TXB2 were assayed by HPLC/ECD and RIA, respectively. RESULTS: MN-9202 inhibited platelet aggregation induced by ADP and thrombin in a concentration-dependent manner. MN-9202 1 mumol.L-1 inhibited release of 5-HT in PRP induced by collagen at 15 mg.L-1 (113 +/- 15 vs 178 +/- 18, P < 0.05), however, MN-9202 did not have effect on 5-HT secreted by high dose of collagen. MN-9202 0.1 and 1 mumol.L-1 blocked extracellular calcium influx and sarcoplasmic calcium release, and the suppression on extracellular calcium influx was more obvious. Furthermore, treatment with MN-9202 0.01, 0.1, and 1 mumol.L-1 markedly decreased ADP-induced TXB2 (pg/10(8) platelet) release from PRP (906 +/- 200, 881 +/- 131, and 793 +/- 169 vs 1264 +/- 202, P < 0.01). CONCLUSION: MN-9202 acts as an effective Ca2+ antagonist and blocks platelet activation by inhibiting platelet Ca2+ influx and arachidonic acid metabolism.

Animals↗